Diabetic ketoacidosis

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) may be a complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus

type 2 diabetes mellitus

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may also develop DKA.

Whilst DKA remains a serious condition, mortality rates have decreased from 8% to under 1% in the past 20 years.

Pathophysiology

• DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies
  DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies
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• Absolute or relative insulin deficiency, together with increased counter-regulatory hormones (especially glucagon), drives hepatic gluconeogenesis and glycogenolysis → hyperglycaemia
• Hyperglycaemia exceeds the renal threshold → glycosuria → osmotic diuresis
  • Leads to loss of water and electrolytes (including potassium), explaining the dehydration, tachycardia, and hypotension seen clinically
• Uncontrolled lipolysis releases free fatty acids → hepatic ketogenesis
  • Produces 3-beta-hydroxybutyrate, acetoacetate, and acetone (responsible for fruity breath)
• Accumulation of ketones → metabolic acidosis
  • Drives Kussmaul respiration and contributes to nausea, vomiting, and abdominal pain
• Potassium imbalance:
  • Total body potassium is depleted due to urinary losses from osmotic diuresis and vomiting
  • Serum potassium may initially be normal or raised due to acidosis and insulin deficiency shifting potassium out of cells
  • Potassium levels often fall rapidly with treatment (especially insulin), creating a risk of arrhythmias

The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction

myocardial infarction

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.

Features

• abdominal pain
  abdominal pain
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• polyuria, polydipsia, dehydration
• Kussmaul respiration (deep hyperventilation)
• Acetone-smelling breath ('pear drops' smell)

Diagnostic criteria

Management

Main principles of management

• fluid replacement
  • most patients with DKA are deplete around 5-8 litres
  • isotonic saline
    Diabetic ketoacidosis: isotonic saline should be used initially, even if the patient is severely acidotic
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    Importance: 62
    is used initially, even if the patient is severely acidotic
  • please see an example fluid regime below.
• insulin
  • an intravenous infusion should be started at 0.1 unit/kg/hour
    Diabetic ketoacidosis: the IV insulin infusion should be started at 0.1 unit/kg/hour
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    Importance: 92
  • once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
    is in addition to the 0.9% sodium chloride regime
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• correction of electrolyte disturbance
  • serum potassium is often high on admission despite total body potassium being low
  • this often falls quickly following treatment with insulin resulting in hypokalaemia
  • potassium may therefore need to be added to the replacement fluids
  • if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
• long-acting insulin should be continued, short-acting insulin should be stopped
  long-acting insulin should be continued, short-acting insulin should be stopped
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JBDS example of fluid replacement regime for patient with a systolic BP on admission 90mmHg and over

Please note that slower infusion may be indicated in young adults (aged 18-25 years) as they are at greater risk of cerebral oedema.

JBDS potassium guidelines

Resolution

DKA resolution is defined

DKA resolution is defined

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as:

• pH >7.3 and
• blood ketones < 0.6 mmol/L and
• bicarbonate > 15.0mmol/L

Further points

• both the ketonaemia and acidosis should have been resolved within 24 hours
  ketonaemia and acidosis should have been resolved within 24 hours
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  . If this hasn't happened the patient requires senior review from an endocrinologist
• if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin
• the patient should be reviewed by the diabetes specialist nurse prior to discharge

Complications

Complications may occur from DKA itself or the treatment:

• gastric stasis
• thromboembolism
• arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
• iatrogenic due to incorrect fluid therapy: cerebral oedema
  Cerebral oedema is an important complication of fluid resuscitation in DKA, especially in young patients
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  Importance: 85
  *, hypokalaemia, hypoglycaemia
• acute respiratory distress syndrome
• acute kidney injury

* children/young adults are particularly vulnerable to cerebral oedema

Cerebral oedema is an important complication of fluid resuscitation in DKA, especially in young patients

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Importance: 85

following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought

+PassMedicine Notes

Diabetic ketoacidosis (DKA) may be a complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA.

Whilst DKA remains a serious condition, mortality rates have decreased from 8% to under 1% in the past 20 years.

Pathophysiology

• DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies
• Absolute or relative insulin deficiency, together with increased counter-regulatory hormones (especially glucagon), drives hepatic gluconeogenesis and glycogenolysis → hyperglycaemia
• Hyperglycaemia exceeds the renal threshold → glycosuria → osmotic diuresis
• Leads to loss of water and electrolytes (including potassium), explaining the dehydration, tachycardia, and hypotension seen clinically
• Uncontrolled lipolysis releases free fatty acids → hepatic ketogenesis
• Produces 3-beta-hydroxybutyrate, acetoacetate, and acetone (responsible for fruity breath)
• Accumulation of ketones → metabolic acidosis
• Drives Kussmaul respiration and contributes to nausea, vomiting, and abdominal pain
• Potassium imbalance:
• Total body potassium is depleted due to urinary losses from osmotic diuresis and vomiting
• Serum potassium may initially be normal or raised due to acidosis and insulin deficiency shifting potassium out of cells
• Potassium levels often fall rapidly with treatment (especially insulin), creating a risk of arrhythmias

The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.

Features

• abdominal pain
• polyuria, polydipsia, dehydration
• Kussmaul respiration (deep hyperventilation)
• Acetone-smelling breath ('pear drops' smell)

Diagnostic criteria

American Diabetes Association (2009) _ Joint British Diabetes Societies (2013)| Key points

• glucose > 13.8 mmol/l
• pH < 7.30
• serum bicarbonate 10
• ketonaemia_

Key points

• glucose > 11 mmol/l or known diabetes mellitus
• pH < 7.3
• bicarbonate < 15 mmol/l
• ketones > 3 mmol/l or urine ketones ++ on dipstick |

Management

Main principles of management

• fluid replacement
• most patients with DKA are deplete around 5-8 litres
• isotonic saline is used initially, even if the patient is severely acidotic
• please see an example fluid regime below.
• insulin
• an intravenous infusion should be started at 0.1 unit/kg/hour
• once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
• correction of electrolyte disturbance
• serum potassium is often high on admission despite total body potassium being low
• this often falls quickly following treatment with insulin resulting in hypokalaemia
• potassium may therefore need to be added to the replacement fluids
• if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
• long-acting insulin should be continued, short-acting insulin should be stopped

JBDS example of fluid replacement regime for patient with a systolic BP on admission 90mmHg and over

Fluid _ Volume | 0.9% sodium chloride 1L _ 1000ml over 1st hour | 0.9% sodium chloride 1L with potassium chloride _ 1000ml over next 2 hours | 0.9% sodium chloride 1L with potassium chloride _ 1000ml over next 2 hours | 0.9% sodium chloride 1L with potassium chloride _ 1000ml over next 4 hours | 0.9% sodium chloride 1L with potassium chloride _ 1000ml over next 4 hours | 0.9% sodium chloride 1L with potassium chloride _ 1000ml over next 6 hours |

Please note that slower infusion may be indicated in young adults (aged 18-25 years) as they are at greater risk of cerebral oedema.

JBDS potassium guidelines

Potassium level in first 24 hours (mmol/L) _ Potassium replacement in mmol/L of infusion solution| Over 5.5 _Nil| 3.5-5.5 _ 40| Below 3.5 _Senior review as additional potassium needs to be given|

Resolution

DKA resolution is defined as:

• pH >7.3 and
• blood ketones < 0.6 mmol/L and
• bicarbonate > 15.0mmol/L

Further points

• both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn't happened the patient requires senior review from an endocrinologist
• if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin
• the patient should be reviewed by the diabetes specialist nurse prior to discharge

Complications

Complications may occur from DKA itself or the treatment:

• gastric stasis
• thromboembolism
• arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
• iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
• acute respiratory distress syndrome
• acute kidney injury

* children/young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought